Focus on Coronary Artery Disease and Acute Coronary
- Slides: 80
Focus on Coronary Artery Disease and Acute Coronary Syndrome Nancy Lin, RN, MSN
Reading Assignments l Wong’s Nursing Care of infants and children: Cardiomyopathy: pp. 1315 -1317 l Lewis: Angina, CAD & MI: CH 34 Cardiomyopathy: pp. 826 -830 Central venous access devices pp. 309 -312 l Adams & Urban: Pharmacology CH 38: Pharmacotherapy of Angina Pectoris & Myocardial Infarction Vasodilators pp. 597 -599 Antiplatelets, anticoagulants, fibrinolytics pp. 665 -686 Antihyperlipidemic drugs pp. 502 -515
SLO’s l Describe the pharmacologic management of pediatric and adult clients with cardiac problems. l Identify cardiomyopathy, compare and contrast the pathophysiology, signs & symptoms, and nursing & collaborative management of pediatric and adults clients with Dilated cardiomyopathy, Hypertrophic cardiomyopathy, and Restrictive cardiomyopathy. l Discuss nursing management of pediatric and adult patients with central venous access
Lecture Content Angina l Coronary artery disease l Myocardial Infarction l Cardiomyopathy l Cardiac meds l Central venous access Application of the nursing process l
Coronary Artery Disease and Acute Coronary Syndrome l A type of blood vessel disorder l Atherosclerosis l “hardening of arteries”
Coronary Artery Disease and Acute Coronary Syndrome l Cardiovascular diseases l l major cause of death in the United States Heart attacks (Myocardial Infarctions) l leading cause of all cardiovascular disease & deaths
Coronary Artery Disease Etiology and Pathophysiology l Major cause l l Atherosclerosis Focal deposit of cholesterol and lipid Altered endothelial lining C-reactive protein (CRP)
Coronary Artery Disease Etiology and Pathophysiology l Developmental stages: Fatty streaks l l l Earliest lesions Lipid-filled smooth muscle cells Potentially reversible
Coronary Artery Disease Etiology and Pathophysiology l Developmental stages: Fibrous plaque l l Beginning of progressive changes in arterial wall Lipoproteins transport cholesterol & other lipids into arterial intima Fatty streak covered by collagen forming a fibrous plaque Result = narrowing of vessel lumen
Coronary Artery Disease Etiology and Pathophysiology l Developmental stages: Complicated lesion l Continued inflammation l l l plaque instability, ulceration & rupture Platelets accumulate and thrombus forms Increased narrowing or total occlusion of lumen
Collateral Circulation l l Normally exist within coronary circulation Growth & extent of collateral circulation attributed to two factors l Inherited predisposition to develop new vessels (angiogenesis) l Presence of chronic ischemia
Risk Factors for Coronary Artery Disease l Nonmodifiable l Modifiable
Cultural & Ethnic Health Disparities in CAD l l l White, middle-aged men: African Americans: African American women: Native Americans: Hispanics:
Modifiable Contributing Risk Factors l Diabetes Mellitus l l Incidence of CAD 2 to 4 times greater Manifest CAD more freq. at earlier age. • Diabetic women • 5 to 7 x higher risk
Modifiable Contributing Risk Factors: Tobacco Use l l 2 to 6 x higher risk Dec. estrogen levels Risk proportional to number of cigarettes smoked. Chronic exposure to secondhand smoke
Modifiable Contributing Risk Factors: Obesity l l “Apple” figure higher incidence of CAD than “pear” figure Inc. obesity → inc. heart size → inc. myocardial O 2 consumption.
Modifiable Contributing Risk Factors l Psychologic States
CAD Health Promotion l l Identify people at high risk Health-promoting behaviors l Physical fitness § § FITT formula: 30 minutes >5 days/week Regular physical activity contributes to: § Weight reduction § Reduction of >10% in systolic BP § In some men more than women, an increase in HDL cholesterol
CAD Health Promotion l Health-promoting behaviors § Nutritional therapy Therapeutic Lifestyle Changes § Omega-3 fatty acids §
CAD Health Promotion l Health-promoting behaviors l Cholesterol-lowering drug therapy § § § Statins, niacin Bile acid sequestrants Ezetimibe (Zetia)
CAD Health Promotion l Health-promoting behaviors l Antiplatelet therapy § ASA § Clopidogrel (Plavix)
Clinical Manifestations of CAD Chronic Stable Angina l Etiology and Pathophysiology l Reversible (temporary) myocardial ischemia = angina (chest pain) l l O 2 demand > O 2 supply Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis l For ischemia to occur, artery usually 75% or more stenosed
Clinical Manifestations of CAD Chronic Stable Angina l Intermittent chest pain l l occurs over a long period same pattern of onset, duration & intensity of symptoms
Clinical Manifestations of CAD Chronic Stable Angina l Pain usually lasts 3 to 5 minutes l l l Subsides when precipitating factor relieved Pain at rest is unusual ECG reveals ______
Location of Chest Pain (Angina) Fig. 34 -7
Chronic Stable Angina Nursing and Collaborative Management l l Acute Interventions for anginal attack Drug therapy: Goal: ↓ O 2 demand and/or O 2 supply l l l Short-acting nitrates: Sublingual Long-acting nitrates β-Adrenergic blockers Calcium channel blockers Angiotensin-converting enzyme inhibitors ↑
Chronic Stable Angina Nursing and Collaborative Management l Diagnostic Studies l l l l Health history/physical examination Laboratory studies 12 -lead ECG Chest x-ray Echocardiogram Exercise stress test Cardiac catheterization l l Diagnostic Coronary revascularization: Percutaneous coronary intervention (PCI) § Balloon angioplasty § Stent
Placement of a Coronary Artery Stent Fig. 34 -9
Pre- and Post-PCI with Stent Placement Fig. 34 -10
Acute Coronary Syndrome l Ischemia prolonged & not immediately reversible l l l Unstable angina (UA) Non–ST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation (STEMI)
Relationship Between CAD, Chronic Stable Angina, and ACS Fig. 34 -11
Acute Coronary Syndrome Etiology and Pathophysiology l Deterioration of a once stable plaque l rupture thrombus Result l l platelet aggregation Partial occlusion of coronary artery: UA or NSTEMI Total occlusion of coronary artery: STEMI
Coronary Thrombogenesis Secondary to Plaque Deterioration
Clinical Manifestations of ACS Unstable Angina l Unstable angina l l l New in onset Occurs at rest Has a worsening pattern Unpredictable A medical emergency
Clinical Manifestations of ACS Myocardial Infarction (MI) l Result of sustained ischemia (>20 minutes) l l causing irreversible myocardial cell death (necrosis) Necrosis of entire thickness of myocardium takes 4 to 6 hours
Acute Myocardial Infarction Fig. 34 -13
Transmural (Full-Thickness) MI Fig. 34 -14
Clinical Manifestations of ACS Myocardial Infarction l l l Degree of altered function depends on area of heart involved & size of infarct Contractile function of the heart disrupted in areas of myocardial necrosis Most MIs involve left ventricle (LV)
Occlusion of the Left Anterior Descending Coronary Artery, Resulting in MI Fig. 34 -12
Clinical Manifestations of ACS Myocardial Infarction l Pain l l l Total occlusion → anaerobic metabolism and lactic acid accumulation → severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration Heaviness, constriction, tightness, burning, pressure, or crushing Common locations
Clinical Manifestations of ACS Myocardial Infarction l Sympathetic nervous system stimulation l Cardiovascular
Clinical Manifestations of ACS Myocardial Infarction l Sympathetic nervous system stimulation results in l l Release of glycogen Diaphoresis Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch
Clinical Manifestations of ACS Myocardial Infarction l Cardiovascular l l Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO) Crackles Jugular venous distention Abnormal heart sounds S 3 or S 4 l New murmur l
ST segment, T wave, and Q wave changes associated with myocardial ischemia (A), injury (B), and infarction (C).
ECG findings with anterolateral wall myocardial infarction. Note the pathologic Q waves in leads V 1 to V 3, I, and a. Vl, and the ST segment elevation in leads V 2 to V 5 (arrows).
STEMI vs. NSTEMI
Diagnostic Studies Unstable Angina and Myocardial Infarction l l l Detailed health history and physical 12 -lead ECG Serum cardiac markers Coronary angiography Others: Exercise stress testing, echocardiogram
Serum Cardiac Markers After MI Fig. 34 -15
Collaborative Care Acute Coronary Syndrome l Drug therapy l Vasodilators l l Nitrates Antiplatelets l Oral § § l ASA Clopidogrel (Plavix) IV (Glycoprotein IIb/IIIa Inhibitors) § § Abciximab (Reopro) Eptifibatide (Integrilin)
Acute Coronary Syndrome l Drug Therapy l Anticoagulants l Parenteral § § l Heparin Enoxaparin (Lovenox) Oral § Warfarin (Coumadin)
Acute Coronary Syndrome l Fibrinolytic drug therapy l Alteplase (Activase)
Collaborative Care Acute Coronary Syndrome l Emergency management l Emergent PCI
Collaborative Care Acute Coronary Syndrome l Nutritional therapy
Collaborative Care Acute Coronary Syndrome l Coronary surgical revascularization l l l Fail medical management Presence of left main coronary artery or threevessel disease Not a candidate for PCI Failed PCI with ongoing chest pain Coronary artery bypass graft (CABG) surgery Requires cardiopulmonary bypass l Uses arteries and veins for grafts l
CABG Surgery Fig. 34 -16
Collaborative Care Acute Coronary Syndrome l Coronary surgical revascularization l Off-pump coronary artery bypass l l Does not require cardiopulmonary bypass Transmyocardial laser revascularization • Minimally invasive direct coronary artery bypass (MIDCAB) l Alternative to traditional CABG
Complications of Myocardial Infarction l Dysrhythmias l Heart failure l Cardiogenic shock l Papillary muscle dysfunction l Ventricular aneurysm
Complications of Myocardial Infarction l Acute pericarditis
Complications of Myocardial Infarction l Dressler syndrome l l l Pericarditis with effusion & fever Develops 4 to 6 weeks after MI Pericardial (chest) pain Pericardial friction rub Arthralgia
Myocardial Infarction Healing Process l l l Within 24 hours, leukocytes infiltrate area of cell death Enzymes released from dead cardiac cells Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by second or third day
Myocardial Infarction Healing Process l Development of collateral circulation improves areas of poor perfusion l Necrotic zone identifiable by ECG changes and nuclear scanning l 10 to 14 days after MI, scar tissue still weak & vulnerable to stress
Myocardial Infarction Healing Process l l By 6 weeks after MI, scar tissue has replaced necrotic tissue Ventricular remodeling l normal myocardium will hypertrophy and dilate
Sudden Cardiac Death (SCD) l Unexpected death from cardiac causes l l Most deaths occur outside of hospital CAD accounts for about 80% of all SCDs
Sudden Cardiac Death Etiology and Pathophysiology l Abrupt disruption in cardiac function l l loss of CO and cerebral blood flow Death usually within 1 hour of onset of acute symptoms Most caused by ventricular dysrhythmias Occurs less commonly as a result of LV outflow obstruction
Sudden Cardiac Death Etiology and Pathophysiology l Primary risk factors l Left ventricular dysfunction (EF 30%) l Ventricular dysrhythmias following MI Other risk factors l
Sudden Cardiac Death Nursing and Collaborative Management l Psychosocial adaptation l l l “Brush with death” “Time bomb” mentality Possible role changes Driving restrictions l Change in occupation l
Cardiomyopathy (CMP) l l l A group of diseases that directly affect the structural or functional ability of the myocardium. Can lead to cardiomegaly & HF Leading cause of heart transplantation
Cardiomyopathy l l Classified into three major types: Dilated Hypertrophic Restrictive
Dilated Cardiomyopathy l l Most common type of CMP Has genetic link in 30% of cases Characterized by diffuse inflammation & rapid degeneration of myocardial fibers Results in ventricular dilation, systolic function impairment, atrial enlargement & stasis of blood in LV
Nursing & Collaborative Management: Dilated Cardiomyopathy l l l Control HF by enhancing myocardial contractility & dec. afterload Nitrates & loop diuretics to dec. preload ACE inhibitors to reduce afterload
Hypertrophic Cardiomyopathy l l Asymmetric left ventricular hypertrophy without ventricular dilation Four main characteristics: 1. __________ 2. __________ 3. __________ 4. __________ End result: l impaired ventricular filling More common in men ages 30 to 40
Nursing & Collaborative Management: Hypertrophic Cardiomyopathy l l l Goals of intervention: l improve ventricular filling B blockers Ca channel blockers Antidysrhythmics for dysrhythmias Atrioventricular pacing
Restrictive Cardiomyopathy l l Least common Disease of heart muscle that impairs diastolic filling & stretch Systolic function remains unaffected Ventricles resistant to filling & demand high diastolic filling pressures to maintain CO.
Collaborative Therapy: Cardiomyopathy l l Treat underlying cause Drug therapy: Nitrates (except in HCM) B-adrenergic blockers Antidysrhythmics Ace inhibitors Diuretics Digitalis (contraindicated unless used in HCM pts with Atrial fibrillation) Anticoagulants (if indicated)
Patient & Family Teaching Guide: Cardiomyopathy
Are You Ready for a Math Question? ?
Math Question l Order: 250 ml D 5 W with 25, 000 Units Heparin at 2, 050 units/hr. a. How many ml/hr will you set your pump? b. Over how many hours will the 250 ml bag infuse?
References Adams, M. P. , & Urban, C. Q. (2013), Pharmacology: Connections to nursing practice (2 nd Ed. ) Boston: Pearson Education, Inc. Hockenberry, M. J. & Wilson, D. (2015). Wong’s Nursing care of infants and children (10 th ed. ). St. Louis, MO: Mosby. Lewis, S. , Heitkemper, M. & Dirksen, S. (2014). Medical Surgical Nursing: Assessment and Management of Clinical Problems (9 th ed. ). St. Louis, MO: Mosby
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